Risk factors for thromboembolism, the major cause of arterial embolism, include disturbed blood flow (such as in atrial fibrillation and mitral stenosis), injury or damage to an artery wall, and hypercoagulability (such as increased platelet count). Mitral stenosis poses a high risk of forming emboli which may travel to the brain and cause stroke. Endocarditis increases the risk for thromboembolism, by a mixture of the factors above.

Atherosclerosis in the aorta and other large blood vessels is a common risk factor, both for thromboembolism and cholesterol embolism. The legs and feet are major impact sites for these types. Thus, risk factors for atherosclerosis are risk factors for arterial embolisation as well:

- advanced age

- cigarette smoking

- hypertension (high blood pressure)

- obesity

- hyperlipidemia, e.g. hypercholesterolemia, hypertriglyceridemia, elevated lipoprotein (a) or apolipoprotein B, or decreased levels of HDL cholesterol)

- diabetes mellitus

- Sedentary lifestyle

- stress

Other important risk factors for arterial embolism include:

- recent surgery (both for thromboembolism and air embolism)

- previous stroke or cardiovascular disease

- a history of long-term intravenous therapy (for air embolism)

- Bone fracture (for fat embolism)

A septal defect of the heart makes it possible for paradoxical embolization, which happens when a clot in a vein enters the right side of the heart and passes through a hole into the left side. The clot can then move to an artery and cause arterial embolisation.

Thrombosis prevention is initiated with assessing the risk for its development. Some people have a higher risk of developing thrombosis and its possible development into thromboembolism. Some of these risk factors are related to inflammation. "Virchow's triad" has been suggested to describe the three factors necessary for the formation of thrombosis: stasis of blood, vessel wall injury, and altered blood coagulation. Some risk factors predispose for venous thrombosis while others increase the risk of arterial thrombosis.

The overall absolute risk of venous thrombosis per 100,000 woman years in current use of combined oral contraceptives is approximately 60, compared to 30 in non-users. The risk of thromboembolism varies with different types of birth control pills; Compared with combined oral contraceptives containing levonorgestrel (LNG), and with the same dose of estrogen and duration of use, the rate ratio of deep venous thrombosis for combined oral contraceptives with norethisterone is 0.98, with norgestimate 1.19, with desogestrel (DSG) 1.82, with gestodene 1.86, with drospirenone (DRSP) 1.64, and with cyproterone acetate 1.88. Venous thromboembolism occurs in 100–200 per 100,000 pregnant women every year.

Regarding family history, age has substantial effect modification. For individuals with two or more affected siblings, the highest incidence rates is found among those ≥70 years of age (390 per 100,000 in male and 370 per 100,000 in female individuals), whereas the highest incidence ratios compared to those without affected siblings occurred at much younger ages (ratio of 4.3 among male individuals 20 to 29 years of age and 5.5 among female individuals 10 to 19 years of age).

The risk of VTE is increased in pregnancy by about five times because of a more hypercoagulable state, a likely adaptation against fatal postpartum hemorrhage. Additionally, pregnant women with genetic risk factors are subject to a roughly three to 30 times increased risk for VTE. Preventative treatments for pregnancy-related VTE in hypercoagulable women were suggested by the ACCP. Homozygous carriers of factor V Leiden or prothrombin G20210A with a family history of VTE were suggested for antepartum LMWH and either LMWH or a vitamin K antagonist (VKA) for the six weeks following childbirth. Those with another thrombophilia and a family history but no previous VTE were suggested for watchful waiting during pregnancy and LMWH or—for those without protein C or S deficiency—a VKA. Homozygous carriers of factor V Leiden or prothrombin G20210A with no personal or family history of VTE were suggested for watchful waiting during pregnancy and LMWH or a VKA for six weeks after childbirth. Those with another thrombophilia but no family or personal history of VTE were suggested for watchful waiting only. Warfarin, a common VKA, can cause harm to the fetus and is not used for VTE prevention during pregnancy.

Evidence supports the use of heparin in people following surgery who have a high risk of thrombosis to reduce the risk of DVTs; however, the effect on PEs or overall mortality is not known. In hospitalized non-surgical patients, mortality decreased but not statistically significant. It does not appear however to decrease the rate of symptomatic DVTs. Using both heparin and compression stockings appears better than either one alone in reducing the rate of DVT.

In hospitalized people who have had a stroke and not had surgery, mechanical measures (compression stockings) resulted in skin damage and no clinical improvement. Data on the effectiveness of compression stockings among hospitalized non-surgical patients without stroke is scarce.

The American College of Physicians (ACP) gave three strong recommendations with moderate quality evidence on VTE prevention in non-surgical patients: that hospitalized patients be assessed for their risk of thromboembolism and bleeding before prophylaxis (prevention); that heparin or a related drug is used if potential benefits are thought to outweigh potential harms; and that graduated compression stockings not be used. As an ACP policy implication, the guideline stated a lack of support for any performance measures that incentivize physicians to apply universal prophylaxis without regard to the risks. Goldhaber recommends that people should be assessed at their hospital discharge for persistent high-risk of venous thrombosis, and that people who adopt a heart-healthy lifestyle might lower their risk of venous thrombosis.

In those with cancer who are still walking about yet receiving chemotherapy, LMWH decreases the risk of VTE. Due to potential concerns of bleeding its routine use is not recommended. For people who are having surgery for cancer, it is recommended that they receive anticoagulation therapy (preferably LMWH) in order to prevent a VTE. LMWH is recommended for at least 7–10 days following cancer surgery, and for one month following surgery for people who have a high risk of VTEs.

In adults who have had their lower leg casted or placed in a brace for more than a week, LMWH decreased the risk of VTEs. LMWH is recommended for adults not in hospital with an above-knee cast and a below-knee cast, and is safe for this indication.

Following the completion of warfarin in those with prior VTE, long term aspirin is beneficial.

The main causes of thrombosis are given in Virchow's triad which lists thrombophilia, endothelial cell injury, and disturbed blood flow.

In the United States, approximately 550,000 people die each year from heart-related arterial embolism and thrombosis. Approximately 250,000 of these individuals are female, and approximately 100,000 of all these deaths are considered premature, that is, prior to the age of average life expectancy.

In 2011, the American College of Physicians (ACP) issued a clinical practice guideline making three strong recommendations based on moderate-quality evidence: that hospitalized patients be assessed for their risk of thromboembolism and bleeding before prophylaxis is started; that heparin or a related drug be used if potential benefits are thought to outweigh potential harms; and that graduated compression stockings not be used. The ACP also drew attention to a lack of support for any performance measures encouraging physicians to apply universal prophylaxis without regard to the risks.

A 2014 Cochrane review found that using heparin in medical patients did not change the risk of death or pulmonary embolism. While its use decreased people's risks of DVTs, it also increased people's risks of major bleeding. The review thus recommended the need to balance risks and benefits.

The 2012 ACCP guidelines for nonsurgical patients recommend anticoagulation for the acutely ill in cases of elevated risk when neither bleeding nor a high risk of bleeding exists. Mechanical prophylaxis is suggested when risks for bleeding and thrombosis are elevated. For the critically ill, either pharmacological or mechanical prophylaxis is suggested depending upon the risk. Heparin is suggested in outpatients with cancer who have solid tumors and additional risk factors for VTE—listed as "previous venous thrombosis, immobilization, hormonal therapy, angiogenesis inhibitors, thalidomide, and lenalidomide"—and a low risk of bleeding.

About 90% of emboli are from proximal leg deep vein thromboses (DVTs) or pelvic vein thromboses. DVTs are at risk for dislodging and migrating to the lung circulation. The conditions are generally regarded as a continuum termed "venous thromboembolism" (VTE).

The development of thrombosis is classically due to a group of causes named Virchow's triad (alterations in blood flow, factors in the vessel wall and factors affecting the properties of the blood). Often, more than one risk factor is present.

- "Alterations in blood flow": immobilization (after surgery), injury, pregnancy (also procoagulant), obesity (also procoagulant), cancer (also procoagulant)

- "Factors in the vessel wall": surgery, catheterizations causing direct injury ("endothelial injury")

- "Factors affecting the properties of the blood" (procoagulant state):

- Estrogen-containing hormonal contraception

- Genetic thrombophilia (factor V Leiden, prothrombin mutation G20210A, protein C deficiency, protein S deficiency, antithrombin deficiency, hyperhomocysteinemia and plasminogen/fibrinolysis disorders)

- Acquired thrombophilia (antiphospholipid syndrome, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria)

- Cancer (due to secretion of pro-coagulants)

The major cause of acute limb ischaemia is arterial thrombosis (85%), while embolic occlusion is responsible for 15% of cases. In rare instances, arterial aneurysm of the popliteal artery has been found to create a thrombosis or embolism resulting in ischaemia.

Pulmonary embolism may be preventable in those with risk factors. People admitted to hospital may receive preventative medication, including unfractionated heparin, low molecular weight heparin (LMWH), or fondaparinux, and anti-thrombosis stockings to reduce the risk of a DVT in the leg that could dislodge and migrate to the lungs.

Following the completion of warfarin in those with prior PE, long-term aspirin is useful to prevent recurrence.

Embolism can be classified as to where it enters the circulation either in arteries or in veins. Arterial embolism are those that follow and, if not dissolved on the way, lodge in a more distal part of the systemic circulation. Sometimes, multiple classifications apply; for instance a pulmonary embolism is classified as an arterial embolism as well, in the sense that the clot follows the pulmonary artery carrying deoxygenated blood away from the heart. However, pulmonary embolism is generally classified as a form of venous embolism, because the embolus forms in veins, e.g. deep vein thrombosis.

Arterial embolism can cause occlusion in any part of the body. It is a major cause of infarction, tissue death due to the blockage of blood supply.

An embolus lodging in the brain from either the heart or a carotid artery will most likely be the cause of a stroke due to ischemia.

An arterial embolus might originate in the heart (from a thrombus in the left atrium, following atrial fibrillation or be a septic embolus resulting from endocarditis). Emboli of cardiac origin are frequently encountered in clinical practice. Thrombus formation within the atrium occurs mainly in patients with mitral valve disease, and especially in those with mitral valve stenosis (narrowing), with atrial fibrillation (AF). In the absence of AF, pure mitral regurgitation has a low incidence of thromboembolism.

The risk of emboli forming in AF depends on other risk factors such as age, hypertension, diabetes, recent heart failure, or previous stroke.

Thrombus formation can also take place within the ventricles, and it occurs in approximately 30% of anterior-wall myocardial infarctions, compared with only 5% of inferior ones. Some other risk factors are poor ejection fraction (<35%), size of infarct, and the presence of AF. In the first three months after infarction, left-ventricle aneurysms have a 10% risk of emboli forming.

Patients with prosthetic valves also carry a significant increase in risk of thromboembolism. Risk varies, based on the valve type (bioprosthetic or mechanical); the position (mitral or aortic); and the presence of other factors such as AF, left-ventricular dysfunction, and previous emboli.

Emboli often have more serious consequences when they occur in the so-called "end circulation": areas of the body that have no redundant blood supply, such as the brain and heart.

In people without a detectable thrombophilia, the cumulative risk of developing thrombosis by the age of 60 is about 12%. About 60% of people who are deficient in antithrombin will have experienced thrombosis at least once by age 60, as will about 50% of people with protein C deficiency and about a third of those with protein S deficiency. People with activated protein C resistance (usually resulting from factor V Leiden), in contrast, have a slightly raised absolute risk of thrombosis, with 15% having had at least one thrombotic event by the age of sixty. In general, men are more likely than women to experience repeated episodes of venous thrombosis.

People with factor V Leiden are at a relatively low risk of thrombosis, but may develop thrombosis in the presence of an additional risk factor, such as immobilization. Most people with the prothrombin mutation (G20210A) never develop thrombosis.

In 2004 the first adequately large scale study on the natural history and long-term prognosis of this condition was reported; this showed that at 16 months follow-up 57.1% of patients had full recovery, 29.5%/2.9%/2.2% had respectively minor/moderate/severe symptoms or impairments, and 8.3% had died. Severe impairment or death were more likely in those aged over 37 years, male, affected by coma, mental status disorder, intracerebral hemorrhage, thrombosis of the deep cerebral venous system, central nervous system infection and cancer. A subsequent systematic review of nineteen studies in 2006 showed that mortality is about 5.6% during hospitalisation and 9.4% in total, while of the survivors 88% make a total or near-total recovery. After several months, two thirds of the cases has resolution ("recanalisation") of the clot. The rate of recurrence was low (2.8%).

In children with CVST the risk of death is high. Poor outcome is more likely if a child with CVST develops seizures or has evidence of venous infarction on imaging.

Passage of a clot (thrombus) from a systemic vein to a systemic artery. When clots in systemic veins break off (embolize), they travel first to the right side of the heart and, normally, then to the lungs where they lodge, causing pulmonary embolism. On the other hand, when there is a hole at the septum, either upper chambers of the heart (an atrial septal defect) or lower chambers of the heart (ventricular septal defects), a clot can cross from the right to the left side of the heart, then pass into the systemic arteries as a paradoxical embolism. Once in the arterial circulation, a clot can travel to the brain, block a vessel there, and cause a stroke (cerebrovascular accident).

Thrombophlebitis occurs almost equally between women and men, though males do have a slightly higher possibility. The average age of developing thrombophlebitis, based on analyzed incidents, is 54 for men and 58 for women.

Cerebral venous sinus thrombosis is rare, with an estimated 3-4 cases per million annual incidence in adults. While it may occur in all age groups, it is most common in the third decade. 75% are female. Given that older studies show no difference in incidence between men and women, it has been suggested that the use of oral contraceptives in women is behind the disparity between the sexes. A 1995 report from Saudi Arabia found a doubled incidence at 7 cases per 100,000; this was attributed to the fact that Behçet's disease, which increases risk of CVST, is more common in the Middle East.

A 1973 report found that CVST could be found on autopsy (examination of the body after death) in nine percent of all people. Many of these were elderly and had neurological symptoms in the period leading up to their death, and many suffered from concomitant heart failure.

In children, a Canadian study reported in 2001 that CVST occurs in 6.7 per million annually. 43% occur in the newborn (less than one month old), and a further 10% in the first year of life. Of the newborn, 84% were already ill, mostly from complications after childbirth and dehydration.

Coronary thrombosis is the formation of a blood clot inside a blood vessel of the heart. This blood clot restricts blood flow within the heart. It is associated with narrowing of blood vessels subsequent to clotting. The condition is considered as a type of ischaemic heart disease, also known as a heart attack or myocardial infarction.

Thrombosis in the heart can lead to a myocardial infarction. Coronary thrombosis and myocardial infarction are sometimes used as synonyms, although this is technically inaccurate as the thrombosis refers to the blocking of blood vessels, while the infarction refers to the tissue death due to the consequent loss of blood flow to the heart tissue. The heart contains many connecting blood vessels, and depending upon the location of the thrombosis, the infarction may cause no symptoms. Coronary thrombosis is caused by atherosclerosis.This is when there is build up of cholesterol and fats in the artery walls. So the blood will clot because there isn't enough room for it to flow. The main causes of coronary thrombosis are stress, smoking, high blood pressure, and lack of exercise. Symptoms are sharp pains around the chest area, breathing difficulties, dizziness, and fainting. This is treated by taking Aspirin, Nitrates, or Beta Blockers.

Coronary thrombosis can be a complication associated with drug-eluting stents.

A number of acquired conditions augment the risk of thrombosis. A prominent example is antiphospholipid syndrome, which is caused by antibodies against constituents of the cell membrane, particularly lupus anticoagulant (first found in people with the disease systemic lupus erythematosus but often detected in people without the disease), anti-cardiolipin antibodies, and anti-β-glycoprotein 1 antibodies; it is therefore regarded as an autoimmune disease. In some cases antiphospholipid syndrome can cause arterial as well as venous thrombosis. It is also more strongly associated with miscarriage, and can cause a number of other symptoms (such as livedo reticularis of the skin and migraine).

Heparin-induced thrombocytopenia (HIT) is due to an immune system reaction against the anticoagulant drug heparin (or its derivatives). Though it is named for associated low platelet counts, HIT is strongly associated with risk of venous and arterial thrombosis. Paroxysmal nocturnal hemoglobinuria (PNH) is a rare condition resulting from acquired alterations in the "PIGA" gene, which plays a role in the protection of blood cells from the complement system. PNH increases the risk of venous thrombosis but is also associated with hemolytic anemia (anemia resulting from destruction of red blood cells). Both HIT and PNH require particular treatment.

Hematologic conditions associated with sluggish blood flow can increase risk for thrombosis. For example, sickle-cell disease (caused by mutations of hemoglobin) is regarded as a mild prothrombotic state induced by impaired flow. Similarly, myeloproliferative disorders, in which the bone marrow produces too many blood cells, predispose to thrombosis, particularly in polycythemia vera (excess red blood cells) and essential thrombocytosis (excess platelets). Again, these conditions usually warrant specific treatment when identified.

Cancer, particularly when metastatic (spread to other places in the body), is a recognised risk factor for thrombosis. A number of mechanisms have been proposed, such as activation of the coagulation system by cancer cells or secretion of procoagulant substances. Furthermore, particular cancer treatments (such as the use of central venous catheters for chemotherapy) may increase the risk of thrombosis further.

Nephrotic syndrome, in which protein from the bloodstream is released into the urine due to kidney diseases, can predispose to thrombosis; this is particularly the case in more severe cases (as indicated by blood levels of albumin below 25 g/l) and if the syndrome is caused by the condition membranous nephropathy. Inflammatory bowel disease (ulcerative colitis and Crohn's disease) predispose to thrombosis, particularly when the disease is active. Various mechanisms have been proposed.

Pregnancy is associated with an increased risk of thrombosis. This probably results from a physiological hypercoagulability in pregnancy that protects against postpartum hemorrhage.

The female hormone estrogen, when used in the combined oral contraceptive pill and in perimenopausal hormone replacement therapy, has been associated with a two- to sixfold increased risk of venous thrombosis. The risk depends on the type of hormones used, the dose of estrogen, and the presence of other thrombophilic risk factors. Various mechanisms, such as deficiency of protein S and tissue factor pathway inhibitor, are said to be responsible.

Obesity has long been regarded as a risk factor for venous thrombosis. It more than doubles the risk in numerous studies, particularly in combination with the use of oral contraceptives or in the period after surgery. Various coagulation abnormalities have been described in the obese. Plasminogen activator inhibitor-1, an inhibitor of fibrinolysis, is present in higher levels in people with obesity. Obese people also have larger numbers of circulating microvesicles (fragments of damaged cells) that bear tissue factor. Platelet aggregation may be increased, and there are higher levels of coagulation proteins such as von Willebrand factor, fibrinogen, factor VII and factor VIII. Obesity also increases the risk of recurrence after an initial episode of thrombosis.

It is known that diabetes causes changes to factors associated with coagulation and clotting, however not much is known of the risk of thromboembolism, or clots, in diabetic patients. There are some studies that show that diabetes increases the risk of thromboembolism; other studies show that diabetes does not increase the risk of thromboembolism. A study conducted in the Umea University Hospital, in Sweden, observed patients that were hospitalized due to an thromboembolism from 1997 to 1999. The researchers had access to patient information including age, sex, vein thromboembolism diagnosis, diagnostic methods, diabetes type and medical history. This study concluded that there is, in fact, an increased risk of thromboembolism development in diabetic patients, possibly due to factors associated with diabetes or diabetes itself. Diabetic patients are twice as likely to develop a thromboembolism than are non-diabetic patient. The exact mechanism of how diabetes increases the risk of clot formation remains unclear and could possibly be a future direction for study.

From previous studies, it is known that long distance air travel is associated with high risk of venous thrombosis. Long periods of inactivity in a limited amount of space may be a reason for the increased risk of blood clot formation. In addition, bent knees compresses the vein behind the knee (the popliteal vein) and the low humidity, low oxygen, high cabin pressure and consumption of alcohol concentrate the blood. A recent study, published in the British Journal of Haematology in 2014, determined which groups of people, are most at risk for developing a clot during or after a long flight. The study focused on 8755 frequent flying employees from international companies and organizations. It found that travelers who have recently undergone a surgical procedure or who have a malignant disease such as cancer or who are pregnant are most at risk. Preventative measures before flying may be taken in these at-risk groups as a solution.

Patients who have undergone kidney transplant have a high risk of developing RVT (about 0.4% to 6%). RVT is known to account for a large proportion of transplanted kidney failures due to technical problems (damage to the renal vein), clotting disorders, diabetes, consumption of ciclosporin or an unknown problem. Patients who have undergone a kidney transplant are commonly prescribed ciclosporin, an immunosuppressant drug which is known to reduce renal blood flow, increase platelet aggregation in the blood and cause damage to the endothelial tissue of the veins. In a clinical study conducted by the Nuffield Department of Surgery at the Oxford Transplant Centre, UK, transplant patients were given low doses of aspirin, which has a some anti-platelet activity. There is risk of bleeding in transplant patients when using anticoagulants like warfarin and herapin. Low dosage of aspirin was used as an alternative. The study concluded that a routine low-dose of aspirin in kidney transplant patients who are also taking ciclosporin significantly reduces the risk of RVT development.

Currently laboratory testing is not as reliable as observation when it comes to defining the parameters of Thrombotic Storm. Careful evaluation of possible thrombosis in other organ systems is pertinent in expediting treatment to prevent fatality.Preliminary diagnosis consists of evidence documented with proper imaging studies such as CT scan, MRI, or echocardiography, which demonstrate a thromboembolic occlusion in the veins and/or arteries. Vascular occlusions mentioned must include at least two of the clinic events:

- Deep venous thrombosis affecting one (or more) limbs and/or pulmonary embolism.

- Cerebral vein thrombosis.

- Portal vein thrombosis, hepatic vein, or other intra-abdominal thrombotic events.

- Jugular vein thrombosis in the absence of ipsilateral arm vein thrombosis and in the absence of ipsilateral central venous access.

- Peripheral arterial occlusions, in the absence of underlying atherosclerotic vascular disease,

- resulting in extremity ischemia and/or infarction.

- Myocardial infarction, in the absence of severe coronary artery disease

- Stroke and/or transient ischemic attack, in the absence of severe atherosclerotic disease and at an age less than 60 years.

- Central retinal vein and/or central retinal arterial thrombosis.

- Small vessel thrombosis affecting one or more organs, systems, or tissue; must be documented by histopathology.

In addition to the previously noted vascular occlusions, development of different thromboembolic manifestations simultaneously or within one or two weeks must occur and the patient must have an underlying inherited or acquired hypercoagulable state (other than Antiphospholipid syndrome)

CTEPH is an orphan disease with an estimated incidence of 5 cases per million, but it is likely that CTEPH is under-diagnosed as symptoms are non-specific. Although a cumulative incidence of CTEPH between 0.1% and 9.1% within the first 2 years after a symptomatic PE has been reported, it is currently unclear whether acute symptomatic PE begets CTEPH. Routine screening for CTEPH after PE is not recommended because a significant number of CTEPH cases develops in the absence of previous acute symptomatic PE. In addition, approximately 25% of patients with CTEPH do not present with a clinical history of acute PE. The median age of patients at diagnosis is 63 years (there is a wide age range, but paediatric cases are rare), and both genders are equally affected.

Historically the prognosis for patients with untreated CTEPH was poor, with a 5-year survival of 40 mmHg at presentation. More contemporary data from the European CTEPH registry have demonstrated a 70% 3-year survival in patients with CTEPH who do not undergo the surgical procedure of pulmonary endarterectomy (PEA). Recent data from an international CTEPH registry demonstrate that mortality in CTEPH is associated with New York Heart Association (NYHA) functional class IV, increased right atrial pressure, and a history of cancer. Furthermore, comorbidities such as coronary disease, left heart failure, and chronic obstructive pulmonary disease (COPD) are risk factors for mortality.

A paradoxical embolism, also called a crossed embolism, refers to an embolus which is carried from the venous side of circulation to the arterial side, or vice versa. It is a kind of stroke or other form of arterial thrombosis caused by embolism of a thrombus (blood clot), air, tumor, fat, or amniotic fluid of venous origin, which travels to the arterial side through a lateral opening in the heart, such as a patent foramen ovale, or arteriovenous shunts in the lungs.

The opening is typically an atrial septal defect, but can also be a ventricular septal defect.

Paradoxical embolisms represent two percent of arterial emboli.